Hyperuricemia animal models have long been used for evaluating food-derived anti-hyperuricemia compounds. Fructose and potassium oxonate are commonly used for developing hyperuricemia mouse model. Recent research also developed spontaneous hyperuricemia model by uricase knockout (Uox-/-). In this work, we evaluated 3 kinds of models with the same gene background to illustrate the differences between the treatments. Unlike the uric acid levels in potassium oxonate (224.79 ± 33.62 μmol/L) and Uox-/- groups (458.39 ± 38.29 μmol/L), fructose treatment did not lead to higher serum uric acid level (174.93 ± 30.46 μmol/L) comparing to the control group (153.53 ± 40.96 μmol/L). However, abnormal glycometabolism only developed in the fructose and the Uox-/- group. In addition, anemia, inflammasome and severe renal injury occurred in the Uox-/- group. The Uox-/- mice were then treated with puerarin and allopurinol, and found that puerarin could reduce serum uric acid and alleviated the serious renal damage associated with high uric acid. Thus, the Uox-/- mice could be a suitable model for screening and evaluating anti-hyperuricemia compounds.
Keywords: Fructose; Hyperuricemia; Potassium oxonate; Puerarin; Renal damage; Uric acid; Uricase.
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